The present application relates to an endodontic composition useful for forming a physiologic root end closure in pulpless endodontically treated teeth, including non-vital open apex teeth, and to a method for stimulating formation of said closure using said composition. More particularly, the composition of the invention comprises a buffered collagen gel containing a calcium salt and a phosphate salt. Lugol's solution may be added to the composition to speed gellation.
Various techniques have been advocated for endodontic treatment of non-vital open apex teeth. Most root canals in need of such treatment are irregularly shaped. Thus, techniques using solid or semi-solid root canal fillings, such as silver points, gutta percha cones, and various cements usually leave voids between the filling and the canal wall. Since much of the success of endodontics depends upon an adequate sealing of the apical portion of the root canal, voids must be prevented because canals with no filling material or partially filled canals tend to accept tissue fluids through the apical foramen and become infected.
Another previously used technique makes use of root canal pastes, such as calcium hydroxide-camphorated parachlorophenol paste. Pastes do obviate the problem of voids. However, conventional paste materials, when in contact with periapical tissues and tissue fluids, tend to resorb. They also may stimulate cytotoxic and antigenic inflammatory reactions. These problems are pronounced in non-vital open apex teeth with canals of flaring morphology, and because of the large surface of periapical tissues contactng the root canal filling material. Also, growth of connective tissue into the root canal is usually limited to less than one millimeter and bridging of the apex with calcification is usually incomplete.
The apexification usually occurs slowly where calcium hydroxide is used to induce hard tissue closure of root canal openings and is often incomplete as described in the article by Steiner, J. C., and Van Hassel, J. J.: Experimental Root Apexification in Primates, Oral Surgery 31:409 (1971). An 18 month treatment period is considered by the authors to be an adequate length of time for a satisfactory apical closure. Another group of workers in the field demonstrated that this type of bridging is porous and concluded that a permanent root canal filling should eventually be placed to form a complete seal; see Ham, J. W. Paterson, S. S. and Mitchell, D. F.: Induced Apical Closure of Immature Pulpless Teeth in Monkeys, Oral Surgery 33:438 (1972). Other research indicated that repair at the apex constitutes proliferation of connective tissue with eventual differentiation into a hard tissue bridge; see Dylewski, J. J.: Apical closures of Non-Vital Teeth, Oral Surgery 32:82 (1971).
Still another technique advocated is that of pushing instruments through the apical foramen to stimulate bleeding into the root canal. The resulting clot formation serves as a matrix for connective tissue and capillary ingrowth. Again, ingrowth is usually limited to less than one millimeter and bridging of the apex with calcified material is incomplete.
Another problem with the prior art methods comes from the fact that the canal is divergent toward the apex. This condition makes it very difficult to adequately clean and smooth the walls with instruments. The difficulty in cleansing can result in bacterial contamination existing in the canal at the time the tooth is filled, and bacterial growth under these conditions is known to inhibit apical closure.
In another approach to this problem, decalcified allogenic bone matrix grafts were surgically implanted into root canals and periapical areas of teeth in monkeys. Formation of new cementum within the canals and new bone within the surgically formed bone cavities was observed. While this technique is of interest, it has the drawback that (1) a surgical procedure is required, (2) it requires the use of non-purified material, and (3) the implant does not conform to the shape of the canal.
The bone morphogenic property of decalcified bone matrix has been well-established; see Narang, R. and Wells, H.: Experimental Osteogenesis in Periapical Areas with Decalcified Allogenic Bone Matrix, Oral Surgery 35:136 (1973). The collagen component of the implant is thought to contribute significantly to the osteogenic response. Mesenchymal cells of the recipient tissue migrate to the implant, palisade, and differentiate into osteoblasts, which in turn produce new bone; see Lutwak, L., Singer, F. R. and Urist, M. R.: UCLA Conference, Current Concepts of Bone Metabolism, Annals of Internal Medicine, 80, (1974) and Van de Putte, K. A. and Urist, M. R.: Osteogenesis in the Interior of Intramuscular Implants of Decalcified Bone Matrix, Clinical Orthopaedics and Related Research (edited by DePalma, A. F.) Vol. 43, 270, (J. B. Lippincott Co., Phil. 1965).
Skin derived collagen and bone matrix collagen appear to be similar both structurally and chemically; see Nimmi, M. E., Metabolic Pathways and Control Mechanisms Involved in the Biosynthesis and Turnover of Collagen in Normal and Pathological Connective Tissues, J. Oral Path. 2:175 (1973). Skin derived collagen sponges have been implanted into debrided osteomyelitic infection sites resulting in accelerated wound healing; see Chvaoil, M., Kronenthal, R. L., and Van Winkle, W., Jr.: Internat Rev. of Conn. Tissue Res. (edit. by Hall, D. A., and Jackson D. S.) Vol. 6: (Academic Press, N.Y. 1973). Skin derived collagen has also been used with CaCl.sub.2 and K.sub.2 HPO.sub.4 to form hydoxyapatite crystals; see Termine, J. D., and Posner, A. S., Calcium Phosphate Formation in Vitro, Arch. of Biochem. and Biophysics 140, 307 (1970). In vitro studies have demonstrated the dynamics of fibroblast migration along the micro-scaffold provided by the fibrils within a collagen gel; see Maroudas, N. G.: Chemical and Mechanical Requirements for Fibroblast Adhesion, Nature, 244, 353 (1973).